It is well known from the state of the art that each hair follicle undergoes repeated cycles characterized by three stages: growth (anagen), involution (catagen), and resting phase (telogen). During anagen, the longest phase of the cycle, the follicle reaches its maximum growth potential. The matrix cells actively proliferate giving origin to the main anatomical structures of the follicle: the internal root sheath and the hair shaft (composed by cuticula, cortex and medulla). During catagen much of the follicle undergoes programmed cell death that causes the disassembling of the hair bulb (the hair shaft factory) and the reduction of the hair follicle size. At the end of this phase the hair follicle enters telogen, during which the proliferative and biochemical activity of the organ reaches its lowest level.
The duration of the various stages of the life cycle of the hair follicle varies with the age of the individual and the region of the body where the hair grows. For example, whereas in the scalp region anagen lasts from two to eight years, compared with a period of a few weeks for the catagen stage and a few months for the telogen stage, in the eyebrow region the anagen stage lasts for only a few months. This time ratio also determines the percentage of hair follicles which are present, on average, in the various stages of the cycle, for each region of the body. The durations of the various stages of the cycle, as well as the transition between one stage and another, are regulated by complex biological interactions, the mechanisms of which are not entirely clear, between the various parts of the hair follicle and between the follicle and the surrounding epithelial environment. It is, however, known that these stages are affected by many endogenous and exogenous factors which act, directly or indirectly, on the hair follicle to lengthen or shorten the duration of each individual stage.
Many attempts have been made to identify factors that cause an early entry into the catagen phase or disorders of the hair follicle, and to provide actives to fight these symptoms, however, with little success so far. It is believed that an active that promotes hair growth and, particularly, fights truly successfully against hair loss, would double the existing market for men's hair care products world-wide.
The present invention relates to the problems explained above and, more particularly, it aims to propose a treatment to fight hair loss based on increasing the anagen period of the hair follicles cycle and, as a consequence, on retarding the entry into catagen. At the same time, the growth of the hair follicles should be stimulated along with an increase of the number of cells in the proliferative stage. Finally, the new compositions should avoid any increase in cell apoptosis.
The invention discloses novel biological activities of Pargyline, yet known as Monoamine Oxydase Inhibitor (MAOI). As discussed below in details, the MAOIs are traditionally exploited for their activity on MAOs located in different tissues of the human body, but no activity on hair follicle metabolism has been disclosed so far.
In this context, attention is drawn to US 2004/0241220 A1 (DiSanto), dealing with the use of the S(+) enantiomer of desmethylselegiline (N-methyl-N-(prop-2-yinyl)-2-aminophenylpropane) [“S(+)DMS”]
for the treatment of Selegiline-responsive diseases in general and for the treatment of narcolepsy in particular. The specification [0005]-[0006] refers to the fact that Selegilines are well-known MAO inhibitors. In section [0030], the “Selegiline responsive diseases”, which are related to neuronal disorders or trauma, are listed and, among these, also alopecia is mentioned. However, the considered application bases all disclosed novel effects on the Selegiline's activity on the nervous system.
In the present invention, on the contrary, the disclosed effects have been studied on hair follicles excised and maintained in organ culture in order to prevent influences related to the metabolism of other tissues or modulated via the general metabolism of the donor. The described direct effects on the metabolic processes of the isolated hair follicle do not find any reference in the prior art.